Abstract: SA-PO0695
Similar Onset, Divergent Outcomes: Two Cases of Thrombotic Microangiopathy Masquerading as Fulminant Myocarditis
Session Information
- Glomerular Diseases: Complement-Mediated Glomerulopathies and Infection-Related GN
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Zhao, Tongxin, Center for Kidney Diseases, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China
- Liu, Jin, Center for Kidney Diseases, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China
- Fang, Yi, Center for Kidney Diseases, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China
- He, Weichun, Center for Kidney Diseases, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China
Introduction
Fulminant myocarditis typically develops within 2 weeks of preceding viral infection, and can cause cardiogenic shock, even sudden death. Complement-mediated thrombotic microangiopathy (TMA), i.e., atypical hemolytic uremic syndrome (aHUS), may present with similar clinical manifestations when it involves the myocardium, carrying a risk of misdiagnosis and delayed treatment.
Case Description
Two young women developed cardiogenic shock 1-2 days after onset of fever and upper respiratory symptoms, and were admitted to a local hospital ICU with suspected fulminant myocarditis. Both experienced cardiac arrest, and cardiac function recovered after cardiopulmonary resuscitation and ECMO support. Subsequently, they developed acute kidney injury requiring dialysis, and were transferred to our department for further treatment. Retrospective review revealed features of TMA including thrombocytopenia, anemia and elevated serum lactate dehydrogenase from onset. Further laboratory findings confirmed microangiopathic hemolytic anemia. Case 1: 38-year-old, 4 weeks post onset. Renal biopsy confirmed TMA, with 25 out of 29 glomeruli showing global sclerosis. Although ADAMTS13 activity detection was not available, the PLASMIC score indicated a low possibility of thrombotic thrombocytopenic purpura (TTP). When Shiga toxin-associated HUS (STEC-HUS) was also excluded, aHUS was considered. Given the low probability of renal recovery, the patient declined complement inhibitor therapy and opted for maintenance dialysis. Case 2: 23-year-old, 3 weeks post onset. TTP was excluded by normal ADAMTS13 activity, and STEC-HUS was ruled out, leading to a diagnosis of aHUS. Elevated serum C5b-9 level indicated uncontrolled complement activation. Prompt eculizumab therapy resulted in marked renal recovery, dialysis independence, and cardiac function improvement. Genetic testing result is pending.
Discussion
These cases illustrate that aHUS can present with dominant cardiovascular collapse mimicking fulminant myocarditis. In patients with cardiogenic shock following prodromal illness who develop TMA, aHUS should be considered. Early recognition and treatment with eculizumab may prevent permanent organ failure.